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What Does Honk Stand For In Diabetes?

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  1. olivo

    i went for my 35 wk check - am on weekly checks due to GD and polyhaydramnios - on thurs. there were ketones in my urine - what does that mean exactly?

  2. becksydee

    i had ketones in my urine when i went for my checkup (34wks) on monday - they wouldn't let me leave until it had been investigated so sounds like you got off lightly!
    it basically means that your body has stopped burning glucose as fuel and is burning fat & protein instead (ketosis) - in extreme cases it can mean you're suffering from ketoacidosis which is quite serious (& is the condition that the midwife/consultant would be worried about if they found ketones). it's diagnosed by testing blood gases & treated with IV fluids (due to dehydration) and insulin. if you had it, you would probably be feeling really rather ill (nausea, vomiting, stomach pain etc) and would also probably have smelly breath.

  3. notevenamousie

    EITHER that you've not been eating enough or you've not been drinking enough. Possibly both.

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Hyperosmolar Non Ketotic Hypergycaemic Coma (honk) - Deranged Physiology

Hyperosmolar Non Ketotic Hypergycaemic Coma (HONK) Though a distinction is being made between diabetic ketoacidosis and HONK, the two really form a part of the same disease spectrum. Some ketoacidosis is present in HONK, and some hyperosmolarity is present in DKA. However, different mechanisms are at play. HONK is distinct form DKA, and the distinction is not entirely arbitrary, at least from the management point of view. For instance, even though the conditions co-exist 30% of the time, it is possible to treat pure HONK without any supplemental insulin (because there is a satisfactory amount of it in circulation already).DKA is 3 times more common, but HONK has 3 times greater mortality. The chapter on DKA presents a table of discriminating features to help distinguish HONK from DKA. Past CICM SAQs involving HONk have included the following: Question 24 from the first paper of 2017 (management strategy) Question 1 from the second paper of 2016 (DKA vs HONK) Question 17 from the first paper of 2014 (DKA vs HONK) Question 18.1 from the second paper of 2008 (diagnosis and complications) Question 13 from the first paper of 2002 (pathophysiology, complications and treatment) Similarly Continue reading >>

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  1. William F

    I am trying to get into a state of Ketosis right now been strict 85% Fat, and roughly 10% Protein, 5% or less Carbs. (for 4 days now)
    But if I went on a diet of 100% Fat would that induce Nutritional Ketosis faster?
    I am trying to get adapted as rapidly as possible. (Not a very patient person)
    Thanks for any and all information you all can give me.

  2. Kettlebelephant

    100% fat won't give enough glucose and ketones for your brain to function properly also how do you even plan to do that?
    Only drinking olive oil for a couple of days?

  3. Geoff Chafe

    What would you eat? Sticks of butter? Mmmm, butter.

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A lecture on the recognition, pathogenesis, and management of diabetic ketoacidosis and the hyperosmolar hyperglycemic state. Use of the VA and Stanford name/logos is only to indicate my academic affiliation, and neither implies endorsement nor ownership of the included material.

Hyperglycemic Crises In Adult Patients With Diabetes

Go to: PATHOGENESIS The events leading to hyperglycemia and ketoacidosis are depicted in Fig. 1 (13). In DKA, reduced effective insulin concentrations and increased concentrations of counterregulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) lead to hyperglycemia and ketosis. Hyperglycemia develops as a result of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues (12–17). This is magnified by transient insulin resistance due to the hormone imbalance itself as well as the elevated free fatty acid concentrations (4,18). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation in the liver to ketone bodies (β-hydroxybutyrate and acetoacetate) (19), with resulting ketonemia and metabolic acidosis. Increasing evidence indicates that the hyperglycemia in patients with hyperglycemic crises is associated with a severe inflammatory state characterized by an elevation of proinflammatory cytokines (tumor necrosis fac Continue reading >>

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  1. Theodore

    False

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  2. Nicey8

    False. Amino acids condense to form polypeptides and proteins.

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